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• W4382799083 abstract "Genetic and epigenetic alterations, as well as environmental factors contribute to the colorectal carcinogenesis and cancer progression. Particularly, aberrant DNA methylation is recognized as a common molecular feature in human colorectal tumors. However, DNA methylation-based biomarkers are still relatively new, and potential biomarkers are required to further validate them in cancer initiation and progression and for clinical use. We studied the expression and methylation of the TNXB gene in healthy participants and patients with CRC. We evaluated the full biomarker description value of TNXB in CRC, validated TNXB expression and methylation in different biological tissues, and assessed its role as a potential biomarker in CRC. To test the effect of DNA methylation on the TNXB gene expression, we treated the HCT116 cells with siRNA targeted to the TNXB gene. We also determined the effects of TNXB gene on cell proliferation, migration, and the expression of key genes related to the tumorigenic properties. Here, we study epigenetic changes by genome-wide DNA methylation analysis in tumors from patients with colorectal cancer (CRC). We found a total of 73,509 differentially methylated CpG sites (DMCs) (false discovery rate (FDR) < 0.001) in the tumor area when compared to the NAT area. We defined several molecular signaling pathways that were found epigenetically altered in CRC, such as focal adhesion, MAPK, PI3K, and RAS signaling pathways. We also discovered several candidates that are found to be differentially methylated, such as COL4A1, COL11A, ITGA4, OPLAH, MAD1L1, PRDM16, and TNXB. Specifically, our filtered analysis defined TNXB as a potential biomarker and an epimutation in CRC. Overall, TNXB is found to be hypomethylated in the tumor area (p < 0.001), and affect the whole gene, including the body gene and promoter region. Furthermore, this gene was also found to be downregulated in the tumor area (p < 0.001), which was further validated in the adipose tissue, and the TCGA-COAD and TCGA-READ cohorts. Functional analysis in a cell system reported that silencing of TNXB increased cell proliferation and overexpression of TNXB inhibited stemness in CRC. The silencing of TNXB also increased the expression of TGFβ, suggesting a link between TNXB and the regulation of the cell cycle through TGFβ. In summary, our data identify TNXB as an epimutation in CRC. Our observations suggest that altered TNXB methylation and expression contribute to the pathogenesis of CRC by influencing TGFβ. Therefore, targeting TNXB may be a novel mechanism to interfere with cancer initiation and progression." @default.
• W4382799083 created "2023-07-02" @default.
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• W4382799083 date "2023-06-01" @default.
• W4382799083 modified "2023-09-26" @default.
• W4382799083 title "P-51 Epigenome-wide DNA methylation profiling identifies the TNXB gene as a potential epigenetic candidate for colorectal cancer prevention" @default.
• W4382799083 doi "https://doi.org/10.1016/j.annonc.2023.04.107" @default.
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